Nitric oxide regulates bacterial translocation in experimental acute edematous pancreatitis

Çevikel, Mehmet Hakan; Özgün, Hedef; Boylu, Şükrü; Demirkiran, Ahmet Ender; Sakarya, Serhan; Çulhacı, Nil

doi:10.1159/000071772

Cited by 18 publications

(9 citation statements)

References 28 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Some studies showed that the proinflammatory cytokines activate the production of the iNOS, resulting in overproduction of NO, which could promote pancreatic injury [32], [33]. Whereas others reported that NO acts as a biological scavenger and inactivates ROS, which protects pancreatic acinar cells [34] and has also beneficial effects by inhibition of neutrophil accumulation and improvement of microcirculation [35], [36]. Our data showed that after treated with DCQD, the production of NO in pancreatic tissues was increased, accompanying the increase of apoptosis with the decrease of inflammatory cells infiltration and pathological scores in pancreatic tissues.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell

et al. 2012

View full text Add to dashboard Cite

Severity of acute pancreatitis contributes to the modality of cell death. Pervious studies have demonstrated that the herb medicine formula “Dachengqi Decoction” (DCQD) could ameliorate the severity of acute pancreatitis. However, the biological mechanisms governing its action of most remain unclear. The role of apoptosis/necrosis switch within acute pancreatitis has attracted much interest, because the induction of apoptosis within injured cells might suppress inflammation and ameliorate the disease. In this study, we used cerulein (10−8 M)-stimulated AR42J cells as an in vitro model of acute pancreatitis and retrograde perfusion into the biliopancreatic duct of 3.5% sodium taurocholate as an in vivo rat model. After the treatment of DCQD, cell viability, levels of apoptosis and necrosis, reactive oxygen species positive cells, serum amylase, concentration of nitric oxide and inducible nitric oxide syntheses, pancreatic tissue pathological score and inflammatory cell infiltration were tested. Pretreatment with DCQD increased cell viability, induced apoptosis, decreased necrosis and reduced the severity of pancreatitis tissue. Moreover, treatment with DCQD reduced the generation of reactive oxygen species in AR42J cells but increased the concentration of nitric oxide of pancreatitis tissues. Therefore, the regulation of apoptosis/necrosis switch by DCQD might contribute to ameliorating the pancreatic inflammation and pathological damage. Further, the different effect on reactive oxygen species and nitric oxide may play an important role in DCQD-regulated apoptosis/necrosis switch in acute pancreatitis.

show abstract

Section: Discussionmentioning

confidence: 99%

Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell

et al. 2012

View full text Add to dashboard Cite

show abstract

“…The role of NO has been increasingly implicated in the pathophysiology of AP [4,5] and NO may also be involved in the pathogenesis of chronic pancreatitis [6] . Acute necrotizing pancreatitis is associated with raised serum NO levels in its early stage.…”

Section: Introductionmentioning

confidence: 99%

Expression of Nitric Oxide Synthase Isoforms and Nitric Oxide Production in Acute Pancreatitis and Associated Lung Injury

Ang

Adhikari

et al. 2009

Pancreatology

View full text Add to dashboard Cite

“…Takacs et al (33) reported that rats with pancreatitis induced by injection of L-arginine had higher amylase levels, pancreatic weight/body weight ratios, inducible NOS activities, and pancreatic Evans blue dye concentrations than control rats; constitutive NOS activity was also altered in these animals. In addition, Cevikel et al (34) reported that administration of two subcutaneous doses of L-arginine, the main substrate of NO, decreased both the inflammatory changes and bacterial translocation associated with cerulein-induced acute pancreatitis. Also, in the same study it was emphasized that rats that received cerulein plus L-NAME for two consecutive days had higher rates of bacterial translocation and greater pancreatic injury than control rats.…”

Section: Resultsmentioning

confidence: 99%

“…It also probably reduces the release of interferon c from the leukocytes by inhibiting leukocyte migration. Interferon c is partially responsible for the suppression of ROS production (34). The beneficial effects of pentoxifylline are partially dependent on its regulatory effects on microvascular blood flow.…”

Section: Resultsmentioning

confidence: 99%

Liver lipid peroxidation and antioxidant capacity in cerulein-induced acute pancreatitis

Batçıoğlu

Gül

Uyumlu

et al. 2009

Braz J Med Biol Res

View full text Add to dashboard Cite

The aim of this study was to evaluate the role of oxidative damage in pancreatitis-induced hepatic injury. Thirty-five rats were divided into five groups (each of 7 rats): control, cerulein (100 µg/kg body weight), cerulein and pentoxifylline (12 mg/kg body weight), cerulein plus L-NAME (10 mg/kg body weight) and cerulein plus L-arginine (160 mg/kg body weight). The degree of hepatic cell degeneration differed significantly between groups. Mean malondialdehyde levels were 7.00 ± 2.29, 20.89 ± 10.13, 11.52 ± 4.60, 18.69 ± 8.56, and 8.58 ± 3.68 nmol/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Mean catalase activity was 3.20 ± 0.83, 1.09 ± 0.35, 2.05 ± 0.91, 1.70 ± 0.60, and 2.85 ± 0.47 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively, and mean glutathione peroxidase activity was 0.72 ± 0.25, 0.33 ± 0.09, 0.37 ± 0.04, 0.34 ± 0.07 and 0.42 ± 0.1 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Cerulein-induced liver damage was accompanied by a significant increase in tis sue malondialdehyde levels (P < 0.05) and a significant decrease in catalase (P < 0.05) and GPx activities (P < 0.05). L-arginine and pentoxifylline, but not L-NAME, protected against this damage. Oxidative injury plays an important role not only in the pathogenesis of AP but also in pancre atitis-induced hepatic damage.

show abstract

Nitric oxide regulates bacterial translocation in experimental acute edematous pancreatitis

Cited by 18 publications

References 28 publications

Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell

Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell

Expression of Nitric Oxide Synthase Isoforms and Nitric Oxide Production in Acute Pancreatitis and Associated Lung Injury

Liver lipid peroxidation and antioxidant capacity in cerulein-induced acute pancreatitis

Contact Info

Product

Resources

About